Pharmacological effects of Tropisetron

Tropisetron is a highly potent and highly selective antagonist of serotonin 3 (5-HT3) receptors in peripheral neurons and the central nervous system. Anticancer drugs or radiotherapy can stimulate the chromophoric cells of the small intestinal mucosa to release serotonin, induce vomiting reflex, cause nausea and vomiting. Tropisetron selectively inhibits the excitatory presynaptic 5-HT3 receptor excitability of peripheral neurons in this reflex and may have a direct effect on the vagus nerve afferent zone transmitted by the central nervous system 5-HT3 receptor. This dual action blocks the chemical transmission of the neurotransmitter during vomiting and reflex, and thus has a therapeutic effect on vomiting caused by chemotherapy and radiotherapy. Clinical studies have shown that the continuous use of Tropisetron in two to three cancer chemotherapy cycles does not reduce its efficacy.
After oral administration of Tropisetron, absorption from the gastrointestinal tract is rapid and complete, and its absolute bioavailability depends on the dose, which is approximately 60% at a dose of 5 mg and almost 100% at a dose of 45 mg. The oral peak time was 2 ~ 3.5h, the peak plasma concentration was 21.7 ~ 29.0μg / L; the peak plasma concentration was 82 ~ 84μg / L. The effect can be maintained for 24h. About 71% of Tropisetron binds to plasma proteins in a non-specific manner (mainly α1-glycoprotein). The apparent volume of adult distribution is 400-600L; the distribution volume of children is small, about 145L for children under six years old and 265L for children under 15 years old. The half-life of elimination was 7.3 h after intravenous administration and 8.6 h after oral administration; the poor metabolism was 30 h after intravenous administration and 42 h after oral administration.